Ozone: We are studying the mechanisms by which ozone causes pathological damage to pulmonary membrane lipids. We find that ozone causes both ozonolysis of unsaturated polyunsaturated fatty acids (PUFA) and initiates the autoxidation of PUFA. We have shown electron-spin resonance techniques that ozone reacts with PUFA at -78 C to form an unstable intermediate that decomposes at -30 C to form free radicals; we presently postulate the intermediate is a trioxide, LOOOH, formed from the lipid LH. Nitrogen dioxide: By comparison of rates of PUFA autoxidation initiated by NO2 and by a typical organic initiator, we have shown that NO2 reacts with PUFA solely as a free radical initiator. However, we find that NO2 both adds to double bonds and abstracts allylic hydrogens. Cigarette smoke: We find that smoke contains a very high concentration of free radicals (10 to the 14th power per puff). These reactive and highly toxic radicals have a long lifetime and diffuse far from the end of the cigarette. They are inhaled both by smokers and by non-smokers in the vicinity.